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目的:观察阿托伐他汀预处理对大鼠心肌缺血-再灌注损伤(MIRI)超氧化物歧化酶(SOD)和丙二醛(MDA)浓度、心肌细胞内Caspase-3和Nrf2表达的影响,探讨阿托伐他汀的心肌保护作用机制。方法:将40只雄性SD大鼠随机等分为4组:假手术组(A组)、缺血再灌注组(B组)、阿托伐他汀标准剂量预处理组(C组)和阿托伐他汀强化剂量预处理组(D组)。灌胃7d后,第8天制作大鼠在体心肌MIRI模型,结扎左冠状动脉前降支30min,再灌注120min后,用比色法检测心肌中MDA和SOD浓度,Western blot检测活化Caspase-3和Nrf2的表达。结果:与B组比较,C组SOD浓度明显增加(P<0.05),MDA浓度明显减少(P<0.05),Caspase-3表达明显减少(P<0.05),Nrf2表达明显增多(P<0.05);与C组比较,D组SOD浓度、Nrf2表达增加更为明显(P<0.05),MDA、Caspase-3表达减少更为明显(P<0.05)。结论:阿托伐他汀预处理明显增强抗氧化酶活性,抑制指质过氧化,减少细胞凋亡,减轻MIRI损伤,且呈剂量依赖性,表现较强的心肌保护作用,其机制可能与增加心肌Nrf2表达有关。
AIM: To observe the effects of atorvastatin preconditioning on the levels of superoxide dismutase (SOD), malondialdehyde (MDA) and the expression of Caspase-3 and Nrf2 in myocardial ischemia-reperfusion (MIRI) , To investigate atorvastatin myocardial protective mechanism. Methods: Forty male SD rats were randomly divided into 4 groups: sham operation group (A group), ischemia reperfusion group (B group), atorvastatin standard dose pretreatment group (C group) Statin-enhanced dose pretreatment group (group D). After 7 days of intragastric administration, rats were subjected to myocardial MIRI model on the 8th day. The anterior descending branch of the left coronary artery was ligated for 30 minutes and reperfusion for 120 minutes. The contents of MDA and SOD in myocardium were detected by colorimetric assay. The expressions of Caspase-3 And Nrf2 expression. Results: Compared with group B, the concentration of SOD in group C was significantly increased (P <0.05), the concentration of MDA was significantly decreased (P <0.05), the expression of Caspase-3 was significantly decreased and the expression of Nrf2 was significantly increased Compared with group C, the SOD concentration and Nrf2 expression in group D increased more significantly (P <0.05), while the expression of MDA and Caspase-3 decreased more significantly (P <0.05). CONCLUSION: Atorvastatin pretreatment can significantly enhance the activity of antioxidant enzymes, inhibit the lipid peroxidation, reduce the apoptosis and alleviate the MIRI injury in a dose-dependent and protective manner. The mechanism may be related to the increase of myocardium Nrf2 expression.